Pracrical notes on management of non traumatic shock

Approach To
Non Traumatic SHOCK
Dr : Ahmed Adel
Dr : Ibrahim Al mashmali
February 2024
Practical Notes
Supervisor
Associate Professor Of
Internal Medicine and cardiology
Dr : Mohammed Qassem Salah

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Shock is / hypoperfusion at cellular level due to any cause
Shock is a life-threatening circulatory disorder that leads to tissue
hypoxia and a disturbance in microcirculation resulting in global
organ hypoperfusion , multiorgan failure and then death
Deﬁnation

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Shock is a Very serious ( lethal )
condition
If recognized early and treated
properly can be reversible
If delayed or neglected ,
ultimately Be irreversible
In shock cases treate then
investigate
Not every shock is hyptoensive
and not every hypotensive
patient Is shocked
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when you receive any critically ill
patient , you should ask your self
is the patient shocked or in pre
shock stage ! befor doing any
thing
Shock is very common in ICU ,
so you should screen for shock
on all ICU Patients
norepinephrine is vasopressor of
choice in most types
Important Notes

Destributive Shock 50% of all
categories
1 septic shock ( Mc type)
2 Anaphylactic shock
3 neurogenic shock
Hypovolemic Shock 30% of all
categories
1 hemorrhagic
2 non hemorrhagic
Git loss
DKA
Burn
Cardiogenic Shock 19% of all
categories
1 Ischemic inferior MI ( Most serious)
2 Advanced heart failure
3 Dysrhythmia
4 vulvular disease
Obstructive Shock 1% of all
categories
1 Tenstion pneumothorax
2 Cardiac tomponade
3 Massive PE
4 constrictive pericarditis
Causes and categories of shock

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History :
Although the clinical presentation of a patient in shock and the
underlying cause may be quite apparent (e.g., acute myocardial
infarction, anaphylaxis, or hemorrhage),
Post delivery (hypovolemic $ or septic
Post D&C , post abortion , ( septic $
it may be diﬃcult to obtain a history from patients in shock
Some patients in shock may have few symptoms other than
generalized weakness, lethargy, or altered mental status .
Overall , There is no time for history taking , or investigation
Treat Then investigate
Diagnosis of shock

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Shock is a clinical diagnosis
No single physical sign is diagnostic , so , a composite physical
examination findings should be used .
All the following criterions are variable acchording to the specific
situation , but these findings are usually noted in the majority :
Tachycardia >90 Bpm
hypotension SBP < 90 mmhg , MAP < 65
Cold Extrimeties
Oliguria
Altered mental status
Shock index > 1 (HR /SBP) Ex .SBP 90 HR 110. =
Diagnosis of shock

Important notes on ﬁndings of shock
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tachycardia in most shock types
Except
↓ in neurogenic shock
Cardiogenic shock with Heart block
Pt taking B blocker
Cold Extrimeties in most type
Warm in early septic , neurogenic
and anaphylactic shock.
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BP : Is one criterion , actually
increase slightly when cardiac
contractility increases in early shock
and then fall as shock advances
Urine output ↓ Usually .

General principles of shock
Management

Management of Undifferentiated shock
E.D MANAGEMENT
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1# ( in CPR room ) ABCD survey
Identify the need for immediate airway
or breathing intervention
If there is need for immediate airway
intervention → intubate the patient in E.D
2 # Establish vascular access
immediately 2 large bore canula (green
color ) : Simultaneously obtain blood
samples for testing
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3 # Exclude cardiogenic shock ,
then
If adult give 1L NS or RL iv bolus
If child give 30 ml /kg NS or RL in
30min
O2 supply for all pat regardless
the puls oxymeter reading
If suspect anaphylactic or
obstructive shock start speciﬁc
managment in CPR room

ICU Admision ( General rules)
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Befor ICU admision , notify the
doctor in ICU about the available
Facilities eg .. (available
mechanical ventilator ,
monitoring devices ) ect.
In ICU , ONE expeirnced Nurse
and one doctor should be beside
the case (very high risk for
cardiopulmonary arrest )
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IF there's no Suitable conditions,
refer the case to other highly
spicielzed Hospital
# IF there is a suitable conditions
take a very high risk informed
consent from relatives
Then ICU Admision
Don't delay ICU admision

ICU management
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1 # immediate and continous heamodynamic monitoring
Connect the pateient to monitor , MV , infusion sets , Central line , urine catheter
closely monitor CVP → MAP → Svco2 → Lactate level
2# Classify The type of shock
Identify the likely iteology
perform rapid diagnostic studieds
Discuss management plan
medical , surgical , and critical care specialist consultation
3 # monitor results of the serial rutine tests eg .. ABG , lactate level , Svco2 level ,
s cr , electrolytes changes , glycemic Control ..ect
Monitoring and titration of the Vasopressor dose , sedatives doses

ABCDE tenets of shock resuscitation
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The ABCDE tenets of shock resuscitation are
establishing Airway
controlling the work of Breathing
optimizing the Circulation
ensuring adequate oxygen Delivery
achieving End points of resuscitation

1 ) ESTABLISHING THE AIRWAY
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Airway control is best obtained through endotracheal intubation.
Early intubation and controling the work of breathing via MV
Associated with signiﬁcant decrease in mortality.
The combination of sedative agents and positive-pressure
ventilation will often lead to hemodynamic collapse.
To avoid this unwanted situation, initiate volume resuscitation and
vasoactive agents before intubation and positive pressure
ventilation.
N.B : Not all patients need ETT , but It is preferred if there is no
response after the ﬁrst hour of resuscitation

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Rapid sequence intubation : RSI is
the sequential administration of an
induction agent and neuromuscular
blocking agent to facilitate ET
intubation .
Step one : induction agent :
Ketamine 1-2 mg /kg iv bolus
½ minute
Step two : paralytic agents :
Scoline 1.5mg /kg iv bolus
Insert the ETT

Ketamine is the best induction
agent in Shock cases B/C it ↑ BP
1-2 mg /kg iv bolus
Scoline Is the best paralytic agent
due to rapid onset and offset
1.5mg /kg bolus

2) CONTROLLING THE WORK OF BREATHING
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Shock is associated with Signiﬁcant increase in work of breathing and Respiratory
muscles are signiﬁcant consumers of oxygen during shock and contribute to lactate
production
How to control the work of breathing ??
Mechanical ventilation ( assisted , controlled , & synchronized modes ) + sedation
allow for adequate oxygenation, improvement of hypercapnia, decrease the work of
breathing and improve survival.
Shock is associated with a compensatory ↑ in minute ventilation , so , ensure
appropriate initial settings are selected.
Neuromuscular blocking agents ..eg(Rocuruniem )should be considered to further
decrease respiratory muscle oxygen consumption and preserve oxygen delivery to
vital organs .

3) OPTIMIZING THE CIRCULATION
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Fluids and vasopressors.
Fluids : With Exception of cardiogenic shock with pulmonary odema ,
Balanced crystalloids, such as RL or N.S are fluid of choice .
Administer fluid rapidly (over 5 to 20 minutes), in set quantities of 500
or 1000 mL of normal saline, and reassess the patient after each bolus.
Patients with a modest degree of hypovolemia usually require an initial
20 to 30 mL/kg of isotonic crystalloid repated acc to responsiveness
In management of Septic shock up to 6 L in first 12 h may be needed
The Rate of infusion should be acc to CVP (8- 12 cm )
N.B : RL offer a small mortality advantage over normal saline solution

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Central line insertion , CVP Monitoring
Central venous access may aid in
assessing volume status (preload) and
monitoring Scvo2.
It is also the preferred route for the
long-term administration of certain
vasopressor therapy
Target CVP is 8 _ 12 cm
Target Scvo2 more than 70% and less
than 90%
Insertion of central venous access is a
simple procedure , very important step
in management of shock .

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The landmark for the site of entry is the
junction of the middle and medial
thirds of the clavicle.
Successful venous return occurs
typically at a depth of 3 to 5 cm.
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The landmark is the triangle
created by the clavicle , the sternal
and clavicular heads of the SCM .
Insert the needle at a 30- to 45-
degree angle to the skin, 1 cm
below the apex of the triangle

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Vasopressors : Vasopressors are most effective when the vascular space
is “full” CVP (8-12) and least effective when the vascular space is
depleted.
In addition to a vasopressor, an inotrope may be needed to directly
increase CO by increasing contractility and stroke volume.
vasopressor infusion initially through a peripheral IV is unlikely to result in
tissue injury and will improve the time to achieve hemodynamic stability
No mortality beneﬁt in raising mean arterial pressure above the 65 to
70 mm Hg range , Patients with chronic HTN at greater risk of AKI at
lower blood pressures

Drug Noradrenaline Dopamine Dubutamine
Cardiac contractility ++ ++ ++++
Vasoconstriction ++++ ++ Vasodilatation
Cardiac output Slightly ↑ ↑↑ ↑↑↑↑
Side effects Bradycardia * Vomiting
Tachydysrhythmia
Dilated pupile
Vasodilatation at low
doses
Vasodilatation
Hypotension
Tachydysrhythmia
Dose 0.5–50 micro/min
Max 3 mic /kg/min
0.5–20 mic/kg/min 2- 20 mic /kg/min

Noadrenaline
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Noadrenaline is the Vasopressor of
choice In most types of shock
Preparation :
16 mg (4 amp) in 50 ml N.S : 5ml / H
by syringe pump
Titerated every 10min to max 25 ml /h
acc to responsiveness
For example 5ml /h then 10 then 15
If no response at 20 ml /h ,
Add another vasopressors eg .
dopamine

Dopamine
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Dopamine act on 3 receptors acc to the dose (
dopa , beta , Alpha )
IV infusion:2–20 mic/kg/min; titrate by
increments of 5–10 mic/kg/min to desired
response(max50 mic/kg/min)
preparation
( 2amp) 400mg in 50 ml NS
5 ml/hr dopa cause VD
10 ml /hr beta inotropic > VC
20 ml /hr Alpha VC > inotropic
Max 25 ml /h
N.B no beneﬁt from renal dose in AKI

4) ENSURING ADEQUATE OXYGEN DELIVERY
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Control of oxygen consumption is
important in restoring the balance
of oxygen supply and demand
A hyperadrenergic state results
from the compensatory response
to shock, physiologic stress, pain,
cold treatment rooms, and anxiety.
Pain further suppresses
myocardial function, impairing
oxygen delivery and increasing
consumption
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Providing analgesia, muscle
relaxation,
warm covering, anxiolytics,
and even paralytic agents,
when appropriate, decreases
this inappropriate systemic
oxygen consumption .

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Once blood pressure is
stabilized through optimization
of preload and afterload,
oxygen delivery can be
assessed and further
manipulated.
Restore arterial oxygen
saturation to ≥91%.
In shock states, consider a
transfusion of packed red blood
cells to maintain hemoglobin ≥7
grams/dL
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If CO can be assessed, it
should be increased using
volume infusion or inotropic
agents in incremental
amounts until venous oxygen
saturation (mixed venous
oxygen saturation [Svo2] or
Scvo2) and lactate are
normalized.
Sequential examination of
lactate and Svo2 or Scvo2 is a
method to assess adequacy
of a patient’s resuscitation
4) ENSURING ADEQUATE OXYGEN DELIVERY

5) END POINTS OF
RESUSCITATION
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No therapeutic end point is universally
effective,
Noninvasive parameters, such as Bp,
HR, and urine output, may
underestimate the degree of remaining
hypoperfusion , so the use of
additional physiologic end points may
be informative
goal-directed approach of
MAP >65 mm Hg
Cvp of 8 to 12 mm Hg
Scvo2 >70%
urine output >0.5 mL/kg/h
normalized serum lactate

Destributive Shock
Septic shock

Septic shock
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Bacteremia is deﬁned as the
presence of viable bacteria
within the liquid component
of blood (blood infection)
Septicemia is the presence or
multiplying Organism in the
blood
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SIRS is : exaggerated defense
response of the body to a
noxious stressor
Sepsis is SIRS due to
infection

Septic shock
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Sepsis is defined as life-
threatening organ dysfunction
due to dysregulated host
response to infection,
organ dysfunction is defined
as an acute change in total
Sequential Organ Failure
Assessment (SOFA) score of
2 points or greater secondary
to the Infectious cause
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Septic shock is defined by
persisting hypotension requiring
vasopressors to maintain a
mean arterial pressure of 65
mm Hg or higher and a serum
lactate level greater than 2
mmol/L (18 mg/dL) despite
adequate volume resuscitation
noxious stressor

Septic shock
Sepsis : suspected or
proven infection + signs
of systemic inﬂammation
+
organ dysfunction acc to
(SOFA or qSOFA )
Sepsis is SIRS due to infection

systemic inﬂammatory response syndrome
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noxious stressor (infection,
trauma, surgery, acute
inﬂammation, ischemia or
reperfusion, or malignancy, to
localize and then eliminate the
endogenous or exogenous
source of the insult .
To summarize, almost all septic
patients have SIRS, but not all
SIRS patients are septic
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SIRS criteria, any 2 of the
following :
TEMP > 38°C or < than 36°C
Heart rate (HR) > 90 b/min
Respiratory rate (RR) > than 20
breaths/min or arterial carbon
dioxide tension (PaCO) < 32
mm Hg
(WBC) count > than 12,000/µL
or < 4000/µL or with 10%
immature (band) forms

• almost all septic
patients have SIRS, but
not all SIRS patients
are septic

Septic shock
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Septic shock is deﬁned by
persisting hypotension requiring
vasopressors to maintain a
mean arterial pressure of 65
mm Hg or higher and a serum
lactate level greater than 2
mmol/L (18 mg/dL) despite
adequate volume resuscitation
Septic shock is the most
common form of distributive
shock

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6.
Tachycardia >90 Bpm
hypotension SBP < 90
mmhg , MAP < 65
Warm Extrimeties
Oliguria
Altered mental status
Shock index > 1
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SVR ↓↓
CO ↑ early then ↓
Cold Extrimeties is poor
prognosetic sign (irreversible
shock )
Clinical presentation
Septic shock

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General manifestation :
Fever (usually > 38°C , chills, and
rigors
Confusion , Anxiety
Diﬃculty Of breathing
Fatigue and malaise
Nausea and vomiting
Acute confusion state in elderly is
due to sepsis until proved
otherwise
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Acc to the site of infection
Head and neck infections – Severe
headache, neck stiffness, altered
mental status, earache, sore throat,
sinus pain or tenderness, and cervical
or submandibular lymphadenopathy
Chest : Cough (especially if productive)
, pleuritic chest pain, dyspnea
Cardiac – Any new murmur, especially
in patients with a history of injection
or intravenous (IV) drug use
Septic shock

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Abdominal and (GI) infections :
Diarrhea, abdominal pain,
abdominal distention, guarding
or rebound tenderness, and
rectal tenderness or swelling
Pelvic and genitourinary (GU)
infections – Pelvic or ﬂank pain,
adnexal tenderness or masses,
vaginal or urethral discharge,
dysuria, frequency, and urgency
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Skin infections – Petechiae,
purpura, erythema, ulceration,
bullous formation, and
ﬂuctuance
Bone and soft-tissue infections
– Localized limb pain or
tenderness, focal erythema,
edema, and swollen joint,
crepitus in necrotizing
infections, and joint effusions
Septic shock

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CBC WBC >15000 highly suspect bacterial
infection , WBC ≥ 50,000/µL or < 300/µL are
associated with significantly decreased survival
rates .
Hemoglobin concentration dictates oxygen-
carrying capacity in blood, which is crucial in
shock to maintain adequate tissue perfusion.
Platelets, as acute-phase reactants, usually
increase at the onset of any serious stress and are
typically elevated in the setting of inflammation.
However, the platelet count will fall with persistent
sepsis, and disseminated intravascular
coagulation (DIC) may develop.
Low plat is ass with poor prognosis
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CRP titer
Blood culture +VE In 30%
Urine culture , pus culture
Gram stain and culture of secretions
and tissue .
eg, cerebrospinal fluid [CSF], wounds,
respiratory secretions, or other body
fluids)
Coagulation studies
The PT and the aPTT are elevated in
DIC, fibrinogen levels are decreased,
and fibrin split products are increased.
Laboratory findings
Septic shock

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Renal and hepatic functions
S.creatinine level , BUN
ALT, AST , ALP
Bilirubin level
S.Amylase , S.Lypase
Cardiac enzyme
LP , CSF analysis
Blood chemistries
Regularly monitoring of :
1 ) electrolytes
2 ) RBS : hyperglycemia ass with
high mortality
3 ) ABG / VBG . mixed venous
oxygen saturation SvCO²
4) serum lactate is perhaps the best
serum marker for tissue perfusion ,
The higher level the worse prognosis
and Higher mortality
Laboratory Investigation
Septic shock

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Chest x ray & CT
Erect plain abd x ray
Abd U/S
Echocardiography
Septic shock
Imaging studies

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managment discussed Before.
ABCD tenets of shock resuscitation
Early directed goal therapy
Treatment
Septic shock

Management of septic shock
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5.
Surviving Sepsis Campaign recommendations
include :
all within 1 hour
measuring a lactate
obtaining blood culture
starting antibiotics
beginning 30 mL/kg crystalloid for
hypotension or a lactate >4 mmol/L
initiating vasopressors during or after ﬂuid
resuscitation to maintain a mean arterial
pressure >65 mm Hg

Early Goal directed
therapy
A general protocol for early
goal-directed therapy in the
management of severe sepsis
and septic shock

Fluid resuscitation
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The most important variable
process in volume
replacement is determining
whether a patient is volume
responsive
lifting the legs of a supine
patient for 60 seconds;
improved blood pressure
identifies a volume-responsive
patient who will likely benefit
from more fluid.
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Fluid resuscitation is the most
important in treating septic
shock.
Repated doses of 30ml /kg
boluses until the CVP become
8-12 )
assess the need for further
volume expansion with empiric
crystalloid boluses until the
patient fails to demonstrate a
physiologic or hemodynamic
response
When CVP > 8 , check MAP if
<65 mmhg start vasoactive

Vasoactive agent
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norepinephrine, 0.5 to 30
micrograms/min, is the best ﬁrst
choice since the dual α- and β-
adrenergic effects result in
peripheral vasoconstriction and
cardiac inotropy
Dopamine has a higher rate of
complications, most notably
dysrhythmias and failure,
compared with norepinephrine
and is no longer routinely
recommended
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Vasopressin is a second-line
agent and may allow for the
downtitration of the
norepinephrine dose.
Give vasopressin as a constant
infusion at a rate of 0.03 or 0.04
U/min.
Do not titrate the dose, because
higher rates are associated with
vasospasm and high morbidity.

Dopamine
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Dopamine act on 3 receptors acc to the dose (
dopa , beta , Alpha )
IV infusion:2–20 mic/kg/min; titrate by increments
of 5–10 mic/kg/min to desired response(max50
mic/kg/min)
preparation
( 2amp) 400mg in 50 ml NS
5 ml/hr dopa cause VD
10 ml /hr beta inotropic > VC
20 ml /hr Alpha VC > inotropic
Max 25 ml /h
N.B no beneﬁt from renal dose in AKI

Mixed venous oxygen saturation SvCO²
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A ScvO2 < 70% indicates that the oxygen delivery is inadequate
to meet the oxygen uptake in the tissues, either due to
1 decreased cardiac output
2 low hemoglobin,
3 increased oxygen demand in peripheral tissues
increased ScvO2 > 90 % may indicate poor oxygen uptake by
tissues, either due to mmicrocirculation or mitochondrial failure

Adult non
neutropenic
Suspected organisms Antibiotic
No obvious source Staphylococcus aureus,
streptococci,
gram-negative bacilli, others
Imepinem 1g Tds
Or meropenim 1g TDs
Plus vancomycin 15 mg /kg
TDS
Suspected biliary source Aerobic gram-negative bacilli,
enterococci
Tazact 4.5 g QID
Plus Flagyle 15mg /kg loading
then 7.5mg /kg TDS
Suspected pneumonia Streptococcus pneumoniae,
methicillin-resistant S. aureus,
gram-negative bacilli, Legionella
Cefepime 1g TDS
Plus Moxiﬂox 400mg iv od
Plus Vancomycin
Plus Azythromycin 500mg
Antibiotics

Antibiotic
Adult non
neutropenic
Suspected organisms Antibiotic
suspected
intra-abdominal source
Mixture of aerobic and anaerobic
gram-negative bacilli
Imepinem 1g Tds
Or meropenim 1g TDs
Or Tazact 4.5 g QID
Plus Flagyl 15 mg /kg TDS
suspected
urinary source
Aerobic gram-negative bacilli,
enterococci
Levoflox 750 mg iv Od
Or Tazact 4.5 g QID
Or Ceftreaxon 1g BD
Plus gentamycin 1.5 mg /kg
TDS
Neutropenic adults Aerobic gram-negative bacilli,
especially
P
. aeruginosa, S. aureus
Ceftazidem 2 g TDS
Or Cefepime 2g TDS
Or imepiem Or meropenim or
tazact
Plus levoflox 750 if od
Plus vancomycin 1g TDS
Plus fluconazol 400mg iv od

• goal-directed approach of
MAP >65 mm Hg
Cvp of 8 to 12 mm Hg
Scvo2 >70%
urine output >0.5 mL/kg/h
normalized serum lactate

Adjunactive treatment
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Glycemic Control—
Rigid control of hyperglycemia has been
shown toimprove outcome, likely by reducing
the incidence of sepsis induced multiple-
organ failure.
reduce the length of stay in the ICU,
decrease antibiotic use,Reduce the incidence
and duration of critical-illness polyneuropathy,
and reduce the number of ventilator days.
Glucose control may be provided with either
a glucose concentration–dependent dose
(“sliding scale”) or a constant infusion for
higher serum glucose levels.
Typically, glucose levels should remain below
130 mg/dL.
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Systemic corticosteroids are the
only antiinflammatory agent in
use in clinical practice but
remain controversial .
Hydrocortisone shortens the
time to shock reversal
corticosteroids combined with
vitamin C and thiamine
demonstrated a dramatic
mortality benefit and received
significant media attention .

Sodium Bicarbonate
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Bicarbonate administration
shifts the oxygen hemoglobin dissociation curve to the left,
impairs tissue unloading of hemoglobin-bound oxygen
worsen intracellular acidosis.
However, despite no deﬁnitive clinical trials supporting beneﬁt
but perhaps harm

Destributive Shock
Anaphylactic Shock

Anaphylactic shock
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Anaphylaxis is an acute,
potentially fatal, multiorgan
system reaction caused by the
release of chemical mediators.
Anaphylactic shock is
differentiated from
anaphylactoid reactions in that
the former is a true anamnestic
response in which a sensitized
individual comes in contact with
an antigenic substance , via IgE
Anaphylactoid reaction Without
IgE

Management Principles
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1) treated in Emergency department
(CPR room) with all CPR team ready for
resuscitation
2 ) ﬁrst priority is The Airway
3) Decontamination
4 )Epinephrine is the DOC
5 ) other second line drugs

Airway and Oxygenation
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In severe anaphylaxis,
securing the airway is the ﬁrst
priority.
If angioedoema is suspected
intubate the patient early and
give high ﬂow O2
Following Rapid sequence
intubation guides (RSI)
RSI
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The best induction agent is
ketamine 2 mg /kg Bolus
Followed by scoline 1.5 mg /kg
bolus
Then intubate the patient
Management Principles

Decontamination
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if the causative agent can be
identiﬁed, termination of
exposure should be attempted.
Gastric lavage is not
recommendedfor foodborne
allergens and may be associated
with complications .
In insect stings, remove any
remaining stinging renants
because the stinger continues to
inject venom even if it is detached
from the insect
• If the cause is iv infusion of a
drug , blood transfusion stop
the infusion and detache the
infusion set

Epinephrine Amp ( 1mg in 1ml)
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Epinephrine is the treatment
of choice for anaphylaxis
No signs of CVS collapse
(shock) give epinephrine IM
0.5 mg into the thigh Muscle
repated every 5 min acc to the
response .
IM only if BP normal and no
signs of shock
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If the patient have signs of CVS
collapse (shock) Give epinephrine
iv bolus and infusion
Give 100 micro over 5 min bolus (
mix 1ml of 1:1000 with 9ml NS then
Infuse 1 ml , over 5 min
Infusion 1mg 1amp of 1:1000 in
500 ml NS 0.5ml /min or (30ml /h )
titrate this dose acc to the response

IV crystalloids
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Hypotension is generally the result of distributive
shock and responds well to ﬂuid resuscitation.
A bolus of 1 to 2 L (10 to 20 mL/kg in children) of isotonic
crystalloid solution should be administered concurrently with
epinephrine.

Second line therapy
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Hydrocortisone 250 -500mg
Diphenhydramine (Afeel) 25 -50
mg iV /6h
Treate bronchospasm :
salbutamol And ipratropeum (
Comivent neb )® every 20 min
Magnesium sulphate 2g in 100
ml NS over 20 min
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Glucagon:
In patient taking beta bloker
with refractory hypotention
add :
Glucagon 1 milligram IV every
5 min until hypotension
resolves, followed by 5–15
micrograms/min infusion

Destributive Shock
Neurogenic shock

Neurogenic shock
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Neurogenic shock is produced by
loss of peripheral vasomotor tone
as a result of spinal cord injury,
regional anesthesia
If the level of interruption is below
the midthorax, the remaining
adrenergic system above the level
of injury is activated, resulting in
increased heart rate and
contractility .
If the cardiac sympathetic outﬂow
is affected, bradycardia results

Clinical presentation and diagnosis
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Neurogenic shock isn't spinal
Shock
Extremities are warm above
the level of injury and cool
below.
Blood pressure ↓↓
HR Usually bradycardia , but
tachycardia if below level of
mid thorax
Signs and symptoms of spinal
cord injury and spinal shock
may be present.
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Imaging
CT of spine ( cervical ,
thoracolumbar , and
lumbosacral )
MRI Of spine
CT of the Head

Management
managment
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Establishing Airway :
intubation ?????
Fluids resuscitation : iv N.S
boluses
Vasopressors to keep MAP >
65 mmhg → Nooradrenaline,
adrenaline, or dopamin
Atropine for bradycardia
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Surgical intervention
Rehabilitation

• Cardiogenic shock results from
decreased cardiac output,
leading to inadequate tissue
perfusion despite adequate
circulating volume
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The classic and most
common picture of acute
cardiogenic shock is due to
left ventricular (LV) infarction
and is characterized by the
physiologic triad of
Low cardiac output , high
SVR indices, and ↑↑ PCWP ,
with peripheral VC and
pulmonary edema
Cardiogenic shock

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Cardiogenic shock results in hypoperfusion due to a low
cardiac index; this is not always accompanied by
hypotension.
SBP is usually <90 mm Hg, although it can be higher with
preexisting hypertension or peripheral vasoconstriction
response
Tachycardia Is common unless the patient taking b
blocker Or have heart block Or Rt ventricular MI
Tachypnia is common unless resp muscle fatigue
occurred.
Cold Extrimeties
Cardiogenic shock

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WET and COLD
Lt ventricular Dysfunction :
Chest → Crepitation from pul
odema
Patient Usually pale , Or cyanotic
cool mottled skin .
Cerebral hypoperfusion →
Change mental status
Renal hypoperfusion → Oliguria
CXR→ pulmonary odema
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DRY and cold
isolated RV infarction, the lungs
are spared and venous
congestion occurs,
presenting as increased CVP ,
(Kussmaul sign)
(hepatojugular reﬂux),
enlarged liver,
peripheral edema,
third heart sound (S3)
Cardiogenic shock

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Serum B-type natriuretic
peptide is an indicator of LV
dysfunction but does not
identify the cause
C.Enzymes
C.B.C
S.cr.
S.Lactat
ABG
Investigations

Investigations
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Imaging
Chest X ray
pulmonary congestion or edema, alveolar
infiltrates, and pleural effusion.
Such findings may lag by hours, so their
absence does not exclude cardiogenic
shock.
Preexisting disease can confound the
radiographic appearance, with pulmonary
edema difficult to detect in patients with
severe COPD or ILD
Cardiomegaly is the result of long-
standing myocardial remodeling, and its
presence may not explain the acute
symptoms.
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ECG
STEMI , rhythm, drug toxicity,
electrolyte disturbance..
Echocardiography
To establish cardiogenic shock
causes
Coronary angiography
Swan-Ganz catheterization is
very useful for helping exclude
other causes and types of shock

ED TREATMENT AND STABILIZATION
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Endotracheal intubation is often necessary to
maintain oxygenation and ventilation.
However, the change to positive-pressure
ventilation may further decrease preload and
cardiac output and worsen hypo tension. Be
prepared to administer a ﬂuid bolus in the
absence of severe pulmonary congestion and in
the presence of RV infarction, while also
considering the use of push dose pressors (small
discrete doses of vasopressors) to mitigate the
potential hypotensive effects of intubation.
Keep end-expiratory pressures and tidal volumes
as low as Possible to avoid impairing preload.
Recognize that patients may need additional
vasopressor support after positive-pressure
ventilation.
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Give supplemental oxygen to
keep saturations >91%,
and monitor closely for
impending or acute
respiratory failure that will
require immediate
mechanical ventilation.
Noninvasive ventilation using
CPAP , BiPAP , or high-ﬂow
nasal cannula can provide
temporary airway support.

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Continuous cardiac monitoring
and IV access are necessary.
Correct any hypoxemia,
hypovolemia, rhythm
disturbances, electrolyte
abnormalities , and acid-base
alterations rapidly. Although not
needed immediately,
many beneﬁt from a urinary
drainage catheter to follow
renal output.
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In AMI, give aspirin early (if not
already taking long term) unless
there is an absolute
contraindication.
Do not use α-blockers in
patients with myocardial
infarction in cardiogenic
shockor who are at risk for
cardiogenic shock Withhold
ACEi or other vasodilators
ED TREATMENT AND STABILIZATION

Dobutamin
IV infusion (initial):1–3 mic/kg/min
maintenance:2–40 mic/kg/min , titrate to
desired response
Inotropic only , cause VD
So , is the drug of choice in cardiogenic shock
with heamodynamic stable patient
Can be Used In combination With dopamin in
cardiogenic shock with heamodynamically
unstable patient
Preparation :
( 2 amp )500 mg in 50 ml N.S
Start by 1 ml /h , titrate acc to responsiveness
up to 10 ml /h

Dry and Cold
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Consider a fluid challenge (250–500 mL).
Assess fluid responsiveness; consider additional bolus if the patient
is responsive to fluid.
Reassess for clinical signs of volume overload.
If shock persists, start a vasopressor, ideally, norepinephrine.
if hypoperfusion persists despite fluids and vasopressors
Add inotropic support
Dobutamine
Dopamine

Wet and cold
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Administer inotropic ( dobutamine ) therapy to maintain perfusion.
If shock persists, add a vasopressor (ideally, norepinephrine ).
Once systolic BP is > 90 mm Hg, start diuretic therapy for AHF
Lasix infusion : 200 mg (10 amp of 20mg ) in 50 ml NS 3 ml /h

REFERENCES
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Tintinalli’s Emergency MedicineA
Comprehensive Study Guide Ninth Edition
CURRENT Diagnosis & Treatment
Critical Care THIRD EDITION
Medscape
Amboss
Uptodate
Mayoclinic

Pracrical notes on management of non traumatic shock

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